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Bio X Cell agonistic αcd40 antibody fgk4.5
Agonistic αcd40 Antibody Fgk4.5, supplied by Bio X Cell, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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agonistic αcd40 antibody fgk4.5 - by Bioz Stars, 2026-03

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C57BL/6 mice were harvested 7 days after adjuvanted (poly(I:C)+anti-CD40) vaccine administration or L. monocytogenes (LM)-OVA challenge (LM). Please note that (A–J) are from day 7, and (M–T) are from day 36. (A) Representative CD127 versus KLRG1 staining. (B) Percentage of CD127 + cells. (C) Representative CD127 versus TCF1 staining. (D) Percentage of TCF1 + cells from (C). (E–J) Representative histograms and geometric mean fluorescent intensity (gMFI) quantification for TCF1 (E and F), FOXO1 (G and H), and CD127 (I and J) staining. Dashed lines represent staining of naive (CD44 lo ) T cells. (K and L) CellTrace Violet (CTV)-labeled CD45.1 + OT1s were transferred into WT C57BL/6 recipients, followed by vaccination or LM-ova challenge. At the indicated times, splenic donor OT1 cells were evaluated for TCF1 or T-bet expression within each cell division regardless of harvest time point (K). TCF1 and Tbet gMFI are normalized to an undivided naive (transfer only) control (L). Error bars represent SEM. Data shown are representative of 2 experiments. (M and N) The spleens from C57BL/6 mice were harvested 36 days post vaccination or LM-OVA challenge as in (A). Shown is representative CD127 versus KLRG1 (M) and TCF1 versus CD127 (N) staining. (O–T) Representative histograms and gMFI quantification for TCF1 (O and P), FOXO1 (Q and R), and CD127 (S and T). (U) Fold change in memory T cells from the peak determined by dividing the number of CD127 + TCF1 + memory T cells more than 40 days post vaccination/challenge by the total number of antigen-specific T cells at the peak of the response on day 7. Data from 5 separate experiments are shown. (V–X) OT1 T cell isolated 110 days post vaccination or LM-OVA challenge and evaluated for total cell numbers (U), frequency of IL-2/interferon γ (IFNγ) double-producing T cells (W), and antigen-specific target killing (X) as described in . All data shown are mean ± SEM; n ≥ 4 mice per group, representative of 2–5 independent experiments. Significance was defined by unpaired t test with Welch’s correction and two-way ANOVA, where *p < 0.05, **p < 0.01, ***p < 0.001.

Journal: Cell reports

Article Title: Vaccine adjuvant-elicited CD8+ T cell immunity is co-dependent on T-bet and FOXO1

doi: 10.1016/j.celrep.2023.112911

Figure Lengend Snippet: C57BL/6 mice were harvested 7 days after adjuvanted (poly(I:C)+anti-CD40) vaccine administration or L. monocytogenes (LM)-OVA challenge (LM). Please note that (A–J) are from day 7, and (M–T) are from day 36. (A) Representative CD127 versus KLRG1 staining. (B) Percentage of CD127 + cells. (C) Representative CD127 versus TCF1 staining. (D) Percentage of TCF1 + cells from (C). (E–J) Representative histograms and geometric mean fluorescent intensity (gMFI) quantification for TCF1 (E and F), FOXO1 (G and H), and CD127 (I and J) staining. Dashed lines represent staining of naive (CD44 lo ) T cells. (K and L) CellTrace Violet (CTV)-labeled CD45.1 + OT1s were transferred into WT C57BL/6 recipients, followed by vaccination or LM-ova challenge. At the indicated times, splenic donor OT1 cells were evaluated for TCF1 or T-bet expression within each cell division regardless of harvest time point (K). TCF1 and Tbet gMFI are normalized to an undivided naive (transfer only) control (L). Error bars represent SEM. Data shown are representative of 2 experiments. (M and N) The spleens from C57BL/6 mice were harvested 36 days post vaccination or LM-OVA challenge as in (A). Shown is representative CD127 versus KLRG1 (M) and TCF1 versus CD127 (N) staining. (O–T) Representative histograms and gMFI quantification for TCF1 (O and P), FOXO1 (Q and R), and CD127 (S and T). (U) Fold change in memory T cells from the peak determined by dividing the number of CD127 + TCF1 + memory T cells more than 40 days post vaccination/challenge by the total number of antigen-specific T cells at the peak of the response on day 7. Data from 5 separate experiments are shown. (V–X) OT1 T cell isolated 110 days post vaccination or LM-OVA challenge and evaluated for total cell numbers (U), frequency of IL-2/interferon γ (IFNγ) double-producing T cells (W), and antigen-specific target killing (X) as described in . All data shown are mean ± SEM; n ≥ 4 mice per group, representative of 2–5 independent experiments. Significance was defined by unpaired t test with Welch’s correction and two-way ANOVA, where *p < 0.05, **p < 0.01, ***p < 0.001.

Article Snippet: Mice were immunized via tail vein injection (i.v.) or intraperitoneal injection (i.p.) with the indicated innate receptor agonist(s), with or without αCD40 antibody (40 μg; clone FGK4.5, BioXcell), and detoxified whole chicken OVA protein (150 μg; Sigma).

Techniques: Staining, Labeling, Expressing, Control, Isolation

$CD40 agonist therapy slows the progression of B16F10 tumors. A and B, Pie charts representing the contribution of CD45 + and CD45 – cells in B16F10 tumors ( A ) and the distribution of different immune populations within the CD45 + fraction (averages taken from 7 individual mice; B ). C and D, UMAP plot of 6773 CD45 + immune cells isolated from pools of three subcutaneous B16F10 tumors at a volume of ∼1,055 ± 116.4 mm 3 ( C ) and expression of several key marker genes associated with CD8 + T-cell function ( D ). E–G, Schematic representation ( E ) of the experimental setup indicating intraperitoneal αCD40 administration when tumors reach ≈ 100 mm 3 and the resulting effect of αCD40 administration on B16F10 tumor growth ( F ) and weight ( G ). H, Percentage of live cells that are CD45 + within isotype and αCD40-treated B16F10 tumors. I–Q, Frequency of distinct immune populations within isotype or αCD40 treated B16F10 tumors. R, Percentage of CD8 + T cells that express Ki67, required for cell proliferation. S, Ratio of CD44 + CD62L – effector to CD44 – CD62L + naïve tumor-infiltrating CD8 + T cells. T, Percentage of FoxP3 + cells within CD4 + T cells in treated B16F10 tumors. U, Percentage of CCR8 + Tregs within treated tumors. Representative data from three independent experiments ( n = 7). *, P < 0.05; **, P < 0.01; ****, P < 0.0001.$

Journal: Cancer Research

Article Title: Efficacy of CD40 Agonists Is Mediated by Distinct cDC Subsets and Subverted by Suppressive Macrophages

doi: 10.1158/0008-5472.CAN-22-0094

Figure Lengend Snippet: CD40 agonist therapy slows the progression of B16F10 tumors. A and B, Pie charts representing the contribution of CD45 + and CD45 – cells in B16F10 tumors ( A ) and the distribution of different immune populations within the CD45 + fraction (averages taken from 7 individual mice; B ). C and D, UMAP plot of 6773 CD45 + immune cells isolated from pools of three subcutaneous B16F10 tumors at a volume of ∼1,055 ± 116.4 mm 3 ( C ) and expression of several key marker genes associated with CD8 + T-cell function ( D ). E–G, Schematic representation ( E ) of the experimental setup indicating intraperitoneal αCD40 administration when tumors reach ≈ 100 mm 3 and the resulting effect of αCD40 administration on B16F10 tumor growth ( F ) and weight ( G ). H, Percentage of live cells that are CD45 + within isotype and αCD40-treated B16F10 tumors. I–Q, Frequency of distinct immune populations within isotype or αCD40 treated B16F10 tumors. R, Percentage of CD8 + T cells that express Ki67, required for cell proliferation. S, Ratio of CD44 + CD62L – effector to CD44 – CD62L + naïve tumor-infiltrating CD8 + T cells. T, Percentage of FoxP3 + cells within CD4 + T cells in treated B16F10 tumors. U, Percentage of CCR8 + Tregs within treated tumors. Representative data from three independent experiments ( n = 7). *, P < 0.05; **, P < 0.01; ****, P < 0.0001.

Article Snippet: For CD40 agonist treatments, a single dose of 100 μg of αCD40 (clone: FGK4.5; BioXCell) agonist antibody or rat IgG2a isotype control (clone 2A3; BioXCell) was administered intraperitoneally in a volume of 100 μL HBSS when tumors reached approximately 100 mm 3 .

Techniques: Isolation, Expressing, Marker, Cell Function Assay

$αCD40 therapy in B16F10 is TAM and B-cell independent. A, Growth curve of B16F10 in WT mice after isotype, αCD40, or αCD40/αCD8 treatment. Data from one experiment ( n = 5). B, UMAP showing Cd40 mRNA expression within the CD45 + fraction of B16F10 tumors with volume of 1,055 ±116.4 mm 3 . C, CD40 protein expression across distinct CD45 + cell subsets from 100 mm 3 B16F10 tumors, determined by the change in median fluorescence intensity (ΔMFI) of CD40 stained samples after subtraction of FMO background signal. Representative data from two independent experiments ( n = 5). D, Growth curve of B16F10 in WT mice after isotype, αCD20, αCD40, or αCD20/αCD40 treatment. Representative data from two independent experiments ( n = 5). E and F, Percentage ( E ) of and ratio of ( F ) CD44 + CD62L – effector to CD44 – CD62L + naïve CD8 + T cells within B16F10 tumors after treatment. G, Growth curve of B16F10 in WT mice after isotype, αCD40, αCSF1R, or αCD40/αCSF1R treatment. Representative data from three independent experiments ( n = 7). H and I, Percentage of ( H ) and ratio of ( I ) CD44 + effector to CD62L + naïve CD8 + T cells within B16F10 tumors after treatment. J, Percentage of FoxP3 + cells within CD4 + T cells infiltrating B16F10 tumors after treatment. K, Percentage of CCR8 + Tregs within B16F10 tumors after treatment. ns, nonsignificant; *, P < 0.05; ***, P < 0.001; ****, P < 0.0001.$

Journal: Cancer Research

Article Title: Efficacy of CD40 Agonists Is Mediated by Distinct cDC Subsets and Subverted by Suppressive Macrophages

doi: 10.1158/0008-5472.CAN-22-0094

Figure Lengend Snippet: αCD40 therapy in B16F10 is TAM and B-cell independent. A, Growth curve of B16F10 in WT mice after isotype, αCD40, or αCD40/αCD8 treatment. Data from one experiment ( n = 5). B, UMAP showing Cd40 mRNA expression within the CD45 + fraction of B16F10 tumors with volume of 1,055 ±116.4 mm 3 . C, CD40 protein expression across distinct CD45 + cell subsets from 100 mm 3 B16F10 tumors, determined by the change in median fluorescence intensity (ΔMFI) of CD40 stained samples after subtraction of FMO background signal. Representative data from two independent experiments ( n = 5). D, Growth curve of B16F10 in WT mice after isotype, αCD20, αCD40, or αCD20/αCD40 treatment. Representative data from two independent experiments ( n = 5). E and F, Percentage ( E ) of and ratio of ( F ) CD44 + CD62L – effector to CD44 – CD62L + naïve CD8 + T cells within B16F10 tumors after treatment. G, Growth curve of B16F10 in WT mice after isotype, αCD40, αCSF1R, or αCD40/αCSF1R treatment. Representative data from three independent experiments ( n = 7). H and I, Percentage of ( H ) and ratio of ( I ) CD44 + effector to CD62L + naïve CD8 + T cells within B16F10 tumors after treatment. J, Percentage of FoxP3 + cells within CD4 + T cells infiltrating B16F10 tumors after treatment. K, Percentage of CCR8 + Tregs within B16F10 tumors after treatment. ns, nonsignificant; *, P < 0.05; ***, P < 0.001; ****, P < 0.0001.

Techniques: Expressing, Fluorescence, Staining

$cDC1 function during early tumor growth determines αCD40 response. A, Growth curve of B16F10 in Xcr1 wt/wt and Xcr1 wt/dtr mice after isotype or αCD40 treatment with initial DT administration 24 hours prior to αCD40 administration. Representative data from two independent experiments ( n = 6). B and C, Percentage of ( B ) and ratio of ( C ) CD44 + effector to CD62L + naïve CD8 + T cells infiltrating B16F10 tumors after treatment. D, Growth curve of B16F10 in Xcr1 wt/wt and Xcr1 wt/dtr mice after isotype, αCD40, αCD8, or αCD40/αCD8 treatment with initial DT administration 24 hours prior to αCD40. Representative data from two independent experiments ( n = 6). E, Growth curve of B16F10 in Xcr1 wt/wt and Xcr1 wt/dtr mice after isotype or αCD40 treatment with initial DT administration 24 hours prior to B16F10 tumor implantation. Representative data from two independent experiments ( n = 6). F, Percentage of CD8 + T cells in B16F10 tumors after isotype of αCD40. G, Growth curve of B16F10 tumors in Xcr1 wt/wt and Xcr1 wt/dtr mice after isotype or αCD40/αCSF1R treatment, with initial DT administration 24 hours prior to αCD40. Data from one experiment ( n = 5–9). H and I, UMAP plots of Ccr7 ( H ) and Cd200 ( I ) gene expression within CD45 + fraction of ∼1,055 ±116.4 mm 3 B16F10 tumors. J and K, Percentage of CCR7 + cDC1s ( J ) and cDC2s ( K ) within B16F10 tumors 24 hours after isotype or αCD40. L and M, Percentage of CD200 + cDC1s ( L ) and cDC2s ( M ) within B16F10 tumors 24 hours after isotype or αCD40. N, Median fluorescence intensity quantification of IL12 expression in immune subsets including MigDC, cDC1, and cDC2 after subtraction of FMO signal 24 hours after isotype or αCD40. O, Growth curve of B16F10 tumors in Xcr1 wt/dtr mice after treatment with isotype or αCD40/αCSF1R treatment with DT administration and IL12 neutralization beginning 24 hours prior to αCD40/αCSF1R treatment. Data from one experiment ( n = 5–6). P and Q, Percentage of ( P ) and ratio of ( Q ) CD44 + effector to CD62L + naïve tumor-infiltrating CD8 + T cells after treatments. R and S, Growth curve ( R ) and weights ( S ) of B16F10 tumors in CD45.1 mice reconstituted with Itgax- WT and Itgax- DTR bone marrow after treatment with isotype or αCD40/αCSF1R, with initial DT administration 24 hours prior to αCD40/αCSF1R treatment. Data from one experiment ( n = 6). T and U, Percentage of ( T ) and ratio of ( U ) CD44 + effector to CD62L + naïve CD8 + T cell in B16F10 tumors after treatment. ns, nonsignificant; *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.$

Journal: Cancer Research

Article Title: Efficacy of CD40 Agonists Is Mediated by Distinct cDC Subsets and Subverted by Suppressive Macrophages

doi: 10.1158/0008-5472.CAN-22-0094

Figure Lengend Snippet: cDC1 function during early tumor growth determines αCD40 response. A, Growth curve of B16F10 in Xcr1 wt/wt and Xcr1 wt/dtr mice after isotype or αCD40 treatment with initial DT administration 24 hours prior to αCD40 administration. Representative data from two independent experiments ( n = 6). B and C, Percentage of ( B ) and ratio of ( C ) CD44 + effector to CD62L + naïve CD8 + T cells infiltrating B16F10 tumors after treatment. D, Growth curve of B16F10 in Xcr1 wt/wt and Xcr1 wt/dtr mice after isotype, αCD40, αCD8, or αCD40/αCD8 treatment with initial DT administration 24 hours prior to αCD40. Representative data from two independent experiments ( n = 6). E, Growth curve of B16F10 in Xcr1 wt/wt and Xcr1 wt/dtr mice after isotype or αCD40 treatment with initial DT administration 24 hours prior to B16F10 tumor implantation. Representative data from two independent experiments ( n = 6). F, Percentage of CD8 + T cells in B16F10 tumors after isotype of αCD40. G, Growth curve of B16F10 tumors in Xcr1 wt/wt and Xcr1 wt/dtr mice after isotype or αCD40/αCSF1R treatment, with initial DT administration 24 hours prior to αCD40. Data from one experiment ( n = 5–9). H and I, UMAP plots of Ccr7 ( H ) and Cd200 ( I ) gene expression within CD45 + fraction of ∼1,055 ±116.4 mm 3 B16F10 tumors. J and K, Percentage of CCR7 + cDC1s ( J ) and cDC2s ( K ) within B16F10 tumors 24 hours after isotype or αCD40. L and M, Percentage of CD200 + cDC1s ( L ) and cDC2s ( M ) within B16F10 tumors 24 hours after isotype or αCD40. N, Median fluorescence intensity quantification of IL12 expression in immune subsets including MigDC, cDC1, and cDC2 after subtraction of FMO signal 24 hours after isotype or αCD40. O, Growth curve of B16F10 tumors in Xcr1 wt/dtr mice after treatment with isotype or αCD40/αCSF1R treatment with DT administration and IL12 neutralization beginning 24 hours prior to αCD40/αCSF1R treatment. Data from one experiment ( n = 5–6). P and Q, Percentage of ( P ) and ratio of ( Q ) CD44 + effector to CD62L + naïve tumor-infiltrating CD8 + T cells after treatments. R and S, Growth curve ( R ) and weights ( S ) of B16F10 tumors in CD45.1 mice reconstituted with Itgax- WT and Itgax- DTR bone marrow after treatment with isotype or αCD40/αCSF1R, with initial DT administration 24 hours prior to αCD40/αCSF1R treatment. Data from one experiment ( n = 6). T and U, Percentage of ( T ) and ratio of ( U ) CD44 + effector to CD62L + naïve CD8 + T cell in B16F10 tumors after treatment. ns, nonsignificant; *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.

Techniques: Tumor Implantation, Expressing, Fluorescence, Neutralization

αCSF1R prolongs survival of mice after delayed B16F10 tumor regrowth. A, Growth curve of B16F10 in WT mice after isotype, or αCD40 treatment. Data from one experiment ( n = 5–15). B, Pie chart showing abundance of immune populations within B16F10 tumors during αCD40 response (day 16 after tumor inoculation, tumor volume ≈ 400 mm 3 ) and αCD40 regrowth (day 21 after tumor inoculation, tumor volume ≈ 600 mm 3 ; n = 5). C, Percentage of MMR + TAMs during αCD40 response and regrowth ( n = 3–5). D, Growth curve of B16F10 tumors in WT mice after isotype, αCD40, αCSF1R, or αCD40/αCSF1R treatment. Representative data from two independent experiments ( n = 7). E, Kaplan–Meier survival curve of B16F10 tumor-bearing mice after isotype, αCD40, αCSF1R, or αCD40/αCSF1R treatment, with death indicated as tumor volume >1,500 mm 3 . Representative of two independent experiments ( n = 7). ns, nonsignificant; *, P < 0.05; **, P < 0.01; ***, P < 0.001.

Journal: Cancer Research

Article Title: Efficacy of CD40 Agonists Is Mediated by Distinct cDC Subsets and Subverted by Suppressive Macrophages

doi: 10.1158/0008-5472.CAN-22-0094

Figure Lengend Snippet: αCSF1R prolongs survival of mice after delayed B16F10 tumor regrowth. A, Growth curve of B16F10 in WT mice after isotype, or αCD40 treatment. Data from one experiment ( n = 5–15). B, Pie chart showing abundance of immune populations within B16F10 tumors during αCD40 response (day 16 after tumor inoculation, tumor volume ≈ 400 mm 3 ) and αCD40 regrowth (day 21 after tumor inoculation, tumor volume ≈ 600 mm 3 ; n = 5). C, Percentage of MMR + TAMs during αCD40 response and regrowth ( n = 3–5). D, Growth curve of B16F10 tumors in WT mice after isotype, αCD40, αCSF1R, or αCD40/αCSF1R treatment. Representative data from two independent experiments ( n = 7). E, Kaplan–Meier survival curve of B16F10 tumor-bearing mice after isotype, αCD40, αCSF1R, or αCD40/αCSF1R treatment, with death indicated as tumor volume >1,500 mm 3 . Representative of two independent experiments ( n = 7). ns, nonsignificant; *, P < 0.05; **, P < 0.01; ***, P < 0.001.

Techniques:

Increasing CD8 + T-cell infiltration into LLC tumors does not correlate with improved antitumor effects. A and B, Growth curve ( A ) and tumor weights ( B ) of LLC tumors in WT mice after isotype, αCD40, αCSF1R, and αCD40/αCSF1R treatment. Representative data from three independent experiments ( n = 7). C–E, Percentage of TAMs ( C ), ratio of MHC-II high to MHC-II low TAMs ( D ), and percentage of CD8 + T cells ( E ) within LLC tumors after treatment. F–H, Percentage of neutrophils ( F ), Tregs ( G ), and CD8 + T cells ( H ) within LLC and B16F10 tumors after isotype or αCD40/αCSF1R treatment. I, Percentage of CD8 + T cells within LLC tumors after Flt3L pretreatment and subsequent isotype or αCD40/αCSF1R treatment. Data from one experiment ( n = 7). J, Growth curve of LLC tumors in WT mice after treatment with isotype, αCD40/αCSF1R, Flt3L, or Flt3L/αCD40/αCSF1R. Data from one experiment ( n = 7). K, Percentage of CD8 + T cells within LLC tumors after isotype, αCD25, αCD40/αCSF1R, or αCD40/αCSF1R/αCD25 treatment. Data from one experiment ( n = 7). L, Growth curve of LLC tumors after isotype, αCD25, αCD40/αCSF1R, or αCD40/αCSF1R/αCD25 treatment. M, CXCR2 expression by neutrophils in bone marrow, spleen, blood, and tumor from naïve or LLC tumor-bearing mice. N, Splenocyte proliferation after coculture of splenocytes with day 15 LLC-derived CXCR2 + or CXCR2 – neutrophils measured via 3H-thymidine incorporation (c.p.m., count per minute; n = 3, data pooled from three independent experiments) . O, Growth curve of LLC tumors in Csf3r +/+ or Csf3r –/– after isotype or αCD40/αCSF1R treatment. Representative data from two independent experiments ( n = 7). ns, nonsignificant; *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.

Journal: Cancer Research

Article Title: Efficacy of CD40 Agonists Is Mediated by Distinct cDC Subsets and Subverted by Suppressive Macrophages

doi: 10.1158/0008-5472.CAN-22-0094

Figure Lengend Snippet: Increasing CD8 + T-cell infiltration into LLC tumors does not correlate with improved antitumor effects. A and B, Growth curve ( A ) and tumor weights ( B ) of LLC tumors in WT mice after isotype, αCD40, αCSF1R, and αCD40/αCSF1R treatment. Representative data from three independent experiments ( n = 7). C–E, Percentage of TAMs ( C ), ratio of MHC-II high to MHC-II low TAMs ( D ), and percentage of CD8 + T cells ( E ) within LLC tumors after treatment. F–H, Percentage of neutrophils ( F ), Tregs ( G ), and CD8 + T cells ( H ) within LLC and B16F10 tumors after isotype or αCD40/αCSF1R treatment. I, Percentage of CD8 + T cells within LLC tumors after Flt3L pretreatment and subsequent isotype or αCD40/αCSF1R treatment. Data from one experiment ( n = 7). J, Growth curve of LLC tumors in WT mice after treatment with isotype, αCD40/αCSF1R, Flt3L, or Flt3L/αCD40/αCSF1R. Data from one experiment ( n = 7). K, Percentage of CD8 + T cells within LLC tumors after isotype, αCD25, αCD40/αCSF1R, or αCD40/αCSF1R/αCD25 treatment. Data from one experiment ( n = 7). L, Growth curve of LLC tumors after isotype, αCD25, αCD40/αCSF1R, or αCD40/αCSF1R/αCD25 treatment. M, CXCR2 expression by neutrophils in bone marrow, spleen, blood, and tumor from naïve or LLC tumor-bearing mice. N, Splenocyte proliferation after coculture of splenocytes with day 15 LLC-derived CXCR2 + or CXCR2 – neutrophils measured via 3H-thymidine incorporation (c.p.m., count per minute; n = 3, data pooled from three independent experiments) . O, Growth curve of LLC tumors in Csf3r +/+ or Csf3r –/– after isotype or αCD40/αCSF1R treatment. Representative data from two independent experiments ( n = 7). ns, nonsignificant; *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.

Techniques: Expressing, Derivative Assay

Oxaliplatin synergizes with αCD40/αCSF1R therapy in LLC. A and B, Growth curve of LLC-OVA tumors ( A ) and tumor weights ( B ) from WT mice after isotype, αCD40, αCSF1R, or αCD40/αCSF1R treatment. Representative data from three independent experiments ( n = 7). C, Kaplan–Meier survival curve of LLC-OVA tumor-bearing mice after isotype, αCD40, αCSF1R, or αCD40/αCSF1R treatment, with death indicated as tumor volume >1,500 mm 3 . Data from one experiment ( n = 7). D, Infiltration of CD8 + T cells into LLC-OVA tumors after isotype, αCD40, αCSF1R, or αCD40/αCSF1R treatment. E, Percentage of dextramer + CD8 + T cells within LLC-OVA tumors after treatment. F and G, Infiltration of TAMs into LLC-OVA tumors ( F ) and the ratio of intratumoral MHC-II high to MHC-II low TAMs ( G ). H and I, NF-κB ( H ) or ISRE ( I ) reporter activity in J774 macrophages cell 24 and 48 hours after culturing with LPS alone, or coculturing with LLC cancer cells and subsequent addition of indicated chemotherapeutic compounds ( n = 3). J, Percentage of live CD45 – cells within LLC tumors after treatment with vehicle or oxaliplatin. Representative data from two independent experiments ( n = 5). K and L, Growth curve of LLC tumors ( K ) and tumor weights ( L ) after treatment with vehicle or oxaliplatin and isotype or αCD40/αCSF1R antibodies. Representative data from two independent experiments ( n = 7). M, Percentage of CD8 + T cells infiltrating LLC tumors after treatment. N, Ratio of CD44 + effector to CD62L + naïve tumor-infiltrating CD8 + T cells. O, Percentage of LLC tumor-infiltrating granzyme B + CD8 + T cells. P, Ratio of MHC-II high to MHC-II low TAMs within LLC tumors after treatment. Q, Percentage of FoxP3 + cells within CD4 + T cells infiltrating LLC tumors after treatment. R, Percentage of CCR8 + Tregs within LLC tumors after treatment. ns, nonsignificant; *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.

Journal: Cancer Research

Article Title: Efficacy of CD40 Agonists Is Mediated by Distinct cDC Subsets and Subverted by Suppressive Macrophages

doi: 10.1158/0008-5472.CAN-22-0094

Figure Lengend Snippet: Oxaliplatin synergizes with αCD40/αCSF1R therapy in LLC. A and B, Growth curve of LLC-OVA tumors ( A ) and tumor weights ( B ) from WT mice after isotype, αCD40, αCSF1R, or αCD40/αCSF1R treatment. Representative data from three independent experiments ( n = 7). C, Kaplan–Meier survival curve of LLC-OVA tumor-bearing mice after isotype, αCD40, αCSF1R, or αCD40/αCSF1R treatment, with death indicated as tumor volume >1,500 mm 3 . Data from one experiment ( n = 7). D, Infiltration of CD8 + T cells into LLC-OVA tumors after isotype, αCD40, αCSF1R, or αCD40/αCSF1R treatment. E, Percentage of dextramer + CD8 + T cells within LLC-OVA tumors after treatment. F and G, Infiltration of TAMs into LLC-OVA tumors ( F ) and the ratio of intratumoral MHC-II high to MHC-II low TAMs ( G ). H and I, NF-κB ( H ) or ISRE ( I ) reporter activity in J774 macrophages cell 24 and 48 hours after culturing with LPS alone, or coculturing with LLC cancer cells and subsequent addition of indicated chemotherapeutic compounds ( n = 3). J, Percentage of live CD45 – cells within LLC tumors after treatment with vehicle or oxaliplatin. Representative data from two independent experiments ( n = 5). K and L, Growth curve of LLC tumors ( K ) and tumor weights ( L ) after treatment with vehicle or oxaliplatin and isotype or αCD40/αCSF1R antibodies. Representative data from two independent experiments ( n = 7). M, Percentage of CD8 + T cells infiltrating LLC tumors after treatment. N, Ratio of CD44 + effector to CD62L + naïve tumor-infiltrating CD8 + T cells. O, Percentage of LLC tumor-infiltrating granzyme B + CD8 + T cells. P, Ratio of MHC-II high to MHC-II low TAMs within LLC tumors after treatment. Q, Percentage of FoxP3 + cells within CD4 + T cells infiltrating LLC tumors after treatment. R, Percentage of CCR8 + Tregs within LLC tumors after treatment. ns, nonsignificant; *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.

Techniques: Activity Assay

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